Multiple, objectively measured sleep dimensions including hypoxic burden and chronic kidney disease: findings from the Multi-Ethnic Study of Atherosclerosis
Abstract
<jats:sec><jats:title>Background</jats:title><jats:p>Poor sleep may contribute to
chronic kidney disease (CKD) through several pathways, including hypoxia-induced systemic
and intraglomerular pressure, inflammation, oxidative stress and endothelial dysfunction.
However, few studies have investigated the association between multiple objectively
measured sleep dimensions and CKD.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>We
investigated the cross-sectional association between sleep dimensions and CKD among
1895 Multi-Ethnic Study of Atherosclerosis Sleep Ancillary Study participants who
completed in-home polysomnography, wrist actigraphy and a sleep questionnaire. Using
Poisson regression models with robust variance, we estimated separate prevalence ratios
(PR) and 95% CIs for moderate-to-severe CKD (glomerular filtration rate <60 mL/min/1.73 m<jats:sup>2</jats:sup>
or albuminuria >30 mg/g) among participants according to multiple sleep dimensions,
including very short (≤5 hours) sleep, Apnoea−Hypopnoea Index and sleep apnoea-specific
hypoxic burden (SASHB) (total area under the respiratory event-related desaturation
curve divided by total sleep duration, %min/hour)). Regression models were adjusted
for sociodemographic characteristics, health behaviours and clinical characteristics.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Of
the 1895 participants, mean age was 68.2±9.1 years, 54% were women, 37% were white,
28% black, 24% Hispanic/Latino and 11% Asian. Several sleep metrics were associated
with higher adjusted PR of moderate-to-severe CKD: very short versus recommended sleep
duration (PR=1.40, 95% CI 1.06 to 1.83); SASHB (Box-Cox transformed SASHB: PR=1.06,
95% CI 1.02 to 1.12); and for participants in the highest quintile of SASHB plus sleep
apnoea: PR=1.28, 95% CI 1.01 to 1.63.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Sleep
apnoea associated hypoxia and very short sleep, likely representing independent biological
mechanisms, were associated with a higher moderate-to-severe CKD prevalence, which
highlights the potential role for novel interventions.</jats:p></jats:sec>
Type
Journal articlePermalink
https://hdl.handle.net/10161/21889Published Version (Please cite this version)
10.1136/thoraxjnl-2020-214713Publication Info
Jackson, Chandra L; Umesi, Chizoba; Gaston, Symielle A; Azarbarzin, Ali; Lunyera,
Joseph; McGrath, John A; ... Redline, Susan (n.d.). Multiple, objectively measured sleep dimensions including hypoxic burden and chronic
kidney disease: findings from the Multi-Ethnic Study of Atherosclerosis. Thorax. 10.1136/thoraxjnl-2020-214713. Retrieved from https://hdl.handle.net/10161/21889.This is constructed from limited available data and may be imprecise. To cite this
article, please review & use the official citation provided by the journal.
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Show full item recordScholars@Duke
L. Ebony Boulware
Adjunct Professor in the Department of Medicine
Dr. Boulware is a general internist, physician-scientist and clinical epidemiologist
focused on improving health and health equity for individuals and communities affected
by chronic health conditions such as kidney disease. A national thought leader in
health equity, she has identified patient, clinician, system, and community-level
barriers that result in disparate outcomes for Black and other marginalized individuals.
Using pragmatic trials, she has developed successful interventions, shap
Clarissa Jonas Diamantidis
Associate Professor of Medicine
Joseph Lunyera
Medical Instructor in the Department of Medicine
I am a clinical epidemiologist with a life-long desire to advance our understanding
of etiologic mechanisms of kidney disease, and to advocate for policies that promote
the highest quality care for individuals with kidney disease. Specifically, I am interested
in delineating mechanisms by which exposures in the social environment perpetuate
disparate adverse kidney outcomes such as chronic kidney disease and acute kidney
injury.
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